{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T16:47:03Z","timestamp":1762102023444},"reference-count":54,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2017,5,9]],"date-time":"2017-05-09T00:00:00Z","timestamp":1494288000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"National Science Center, Poland","award":["2011\/01\/B\/NZ6\/00264"],"award-info":[{"award-number":["2011\/01\/B\/NZ6\/00264"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Immunol Cell Biol"],"published-print":{"date-parts":[[2017,9]]},"abstract":"<jats:p>Both complement activation and certain infections (including those with <jats:italic>Yersinia<\/jats:italic> sp.) may contribute to the pathogenesis of juvenile idiopathic arthritis (JIA). We investigated factors specific for the lectin pathway of complement: mannose\u2010binding lectin (MBL), ficolins and MBL\u2010associated serine protease\u20102 (MASP\u20102), in 144 patients and 98 controls. One hundred and six patients had oligoarticular disease and 38 had polyarticular disease. In 51 patients (out of 133 tested), <jats:italic>Yersinia\u2010<\/jats:italic>reactive antibodies were found (JIA Ye<jats:sup>+<\/jats:sup> group). MBL deficiency was significantly more frequent in the JIA Ye<jats:sup>+<\/jats:sup> group than in patients without <jats:italic>Yersinia\u2010<\/jats:italic>reactive antibodies or in controls. Median serum ficolin\u20102 level was significantly lower (and proportion of values deemed ficolin\u20102 insufficient greater) in JIA patients irrespective of their <jats:italic>Yersinia<\/jats:italic> antibody status. The minority (C) allele at \u221264 of the <jats:italic>FCN2<\/jats:italic> gene was less frequent among JIA patients than among control subjects. No differences were found in the frequency of <jats:italic>FCN3<\/jats:italic> gene +1637delC or <jats:italic>MASP2<\/jats:italic> +359 A&gt;G mutations nor for median values of serum ficolin\u20101, ficolin\u20103 or MASP\u20102. However, high levels of serum ficolin\u20103 were under\u2010represented in patients, in contrast to MBL. MBL, ficolin\u20101, ficolin\u20102, ficolin\u20103 and MASP\u20102 were also readily detectable in synovial fluid samples but at a considerably lower level than in serum. Our findings suggest a possible role for the lectin pathway in the pathogenesis of JIA, perhaps secondary to a role in host defence, and indicate that investigations on the specificity of lectin pathway recognition molecules towards specific infectious agents in JIA might be fruitful.<\/jats:p>","DOI":"10.1038\/icb.2017.31","type":"journal-article","created":{"date-parts":[[2017,4,13]],"date-time":"2017-04-13T08:20:31Z","timestamp":1492071631000},"page":"666-675","source":"Crossref","is-referenced-by-count":9,"title":["Lectin pathway factors in patients suffering from juvenile idiopathic arthritis"],"prefix":"10.1111","volume":"95","author":[{"given":"Katarzyna","family":"Kasperkiewicz","sequence":"first","affiliation":[{"name":"Faculty of Biology and Environmental Protection, Department of Microbiology, University of Silesia  Katowice 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